| Hypertensive nephrosclerosis. | |
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MedLine Citation:
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PMID: 18408477 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE OF REVIEW: Hypertensive nephrosclerosis is the second most common cause of end-stage renal disease, however morphologic evidence on the subject is poorly understood. A perennial and vexing problem in understanding kidney hypertension is that correlations between hypertension and vascular and glomerular lesions are only moderate, in part because all of these lesions are present to a greater or lesser degree in the normotensive, aging kidney, with racial differences in severity further compounding the problem. This review looks at newer data on this topic. RECENT FINDINGS: Recent data suggest that there are two different processes leading to glomerulosclerosis, and the combination of the two begins to explain why global correlations between hypertension and morphologic lesions are destined to remain poor. Arterial stiffening with increased pulse pressure down as far as the afferent arteriolar level likely plays an important role in the progression of glomerular lesions. Loss of renal autoregulation with glomerular hypertrophy, hyperfiltration, and focal segmental glomerulosclerosis is now recognized to contribute significantly to nephrosclerosis, particularly in the black population. Ischemic glomerulosclerosis, however, may ultimately be the most important lesion, with consequent hypoxia in the parenchyma beyond, leading to tubular atrophy and interstitial fibrosis. SUMMARY: Hypertensive nephrosclerosis should be seen as a process with two principal modes of glomerular sclerosis, ischemic and hypertrophic, with consequent focal segmental glomerulosclerosis, contributing variably to renal failure according to race and level of hypertension. |
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Authors:
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Gary S Hill |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Current opinion in nephrology and hypertension Volume: 17 ISSN: 1062-4821 ISO Abbreviation: Curr. Opin. Nephrol. Hypertens. Publication Date: 2008 May |
Date Detail:
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Created Date: 2008-04-14 Completed Date: 2008-09-09 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9303753 Medline TA: Curr Opin Nephrol Hypertens Country: England |
Other Details:
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Languages: eng Pagination: 266-70 Citation Subset: IM |
Affiliation:
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European Hospital Georges Pompidou, Paris, France. garyhillparis@aol.com |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Atrophy Blood Pressure Cell Hypoxia Disease Models, Animal Elasticity Fibrosis Glomerular Filtration Rate Homeostasis Humans Hypertension / complications*, pathology, physiopathology Hypertrophy Inflammation Mediators / metabolism Ischemia / complications, physiopathology Kidney Glomerulus / blood supply, pathology, physiopathology* Nephrosclerosis / etiology*, pathology, physiopathology Renal Artery / physiopathology Renal Circulation Transforming Growth Factor beta / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Inflammation Mediators; 0/Transforming Growth Factor beta |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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